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Data-Driven Modeling Of The Causes And Effects Of Interneuronal Dysfunction In Alzheimer’S Disease And Dravet Syndrome, Carlos Perez
Data-Driven Modeling Of The Causes And Effects Of Interneuronal Dysfunction In Alzheimer’S Disease And Dravet Syndrome, Carlos Perez
USF Tampa Graduate Theses and Dissertations
One of the defining features of Alzheimer’s disease (AD) is the increased cleavage of the amyloid precursor protein (APP), causing abnormally high levels of the aggregation form of amyloid beta (Aβ ). Many studies have shown that both AD patients and AD mice models exhibit abnormal network activity, including hypersynchronous excitatory neuron behavior, altered brain rhythms, and in some instances epileptic seizures when exposed to high levels of Aβ In particular, strong experimental evidence suggests that it is the small globular amyloid oligomers (gOs) and curvilinear fibrils (CFs) rather than the more stable, late stage rigid fibrils (RFs) that cause …
Analyzing The Effects Of Ca2+ Dynamics On Mitochondrial Function In Health And Disease, Patrick Toglia
Analyzing The Effects Of Ca2+ Dynamics On Mitochondrial Function In Health And Disease, Patrick Toglia
USF Tampa Graduate Theses and Dissertations
Mitochondria plays a crucial role in cells by maintaining energy metabolism and directing cell death mechanisms by buffering calcium (Ca2+ )from cytosol. Therefore, the Ca2+ overload of mitochondria due to the upregulated cytosolic Ca2+ , observed in many neurological disorders is hypothesized to be a key pathway leading to mitochondrial dysfunction and cell death. In particular, Ca2+ homeostasis disruptions due to Alzheimer’ s disease (AD)-causing presenilins (PS1/PS2) and oligomeric forms of β-amyloid peptides Aβ commonly found in AD patients are presumed to cause detrimental effects on the mitochondria and its ability to function properly. We begin …